This work was supported in part by a grant from the National Institute of Health of the United States government (1R01 DK50567-01A1). The government has certain rights in the invention.
Campylobacter species, primarily C. jejuni and C. coli, are recognized as a major cause of gastrointestinal disease (Skirrow and Blaser, 1992), with between 2 to 8 million cases of campylobacteriosis, and an estimated 200 to 800 deaths per year in the United States. Infection with C. jejuni or C. coli is characterized by the sudden onset of fever, abdominal cramps, and diarrhea with blood and leukocytes. These two species of Campylobacter are very closely related. Though they can be differentiated by a biochemical test, clinically they are associated with virtually the same symptoms, and generally are treated with the same antibiotics. In addition to acute gastrointestinal disease, infection with C. jejuni has been shown to be a frequent antecedent to the development of Guillain-Barre-type polyneuropathy (Kuroki et al., 1991; Yuki et al., 1993). Despite the prevalence and complications associated with Campylobacter infections worldwide, relatively few rapid tests are available for the detection of these organisms.
The binding of many pathogenic bacteria to cells is an important virulence determinant as it prevents the colonizing bacteria from being swept away by mechanical cleansing forces such as peristalsis and fluid flow, and thus permits the subsequent internalization of the bacteria into "non-professional phagocytic cells," i.e., cells that can phagocytize only particles that adhere via a receptor-ligand interaction. As in the case of other intestinal pathogens, the ability of C. coli and C. jejuni to colonize the gastrointestinal tract by binding to epithelial or other cells has been proposed to be essential for their ability to cause disease. Fauchere et al. (Fauchere et al., 1986) found that C. jejuni isolated from individuals with fever and diarrhea exhibited greater binding to epithelial cells than strains isolated from individuals without diarrhea or fever. Studies have been performed to identify and characterize potential Campylobacter adhesins that mediate the organism's attachment to host cells. Possible adhesins include outer membrane proteins (omps) and lipopolysaccharide (McSweegan and Walker, 1986). Others (De Melo and Pechere, 1990) have identified four proteins with apparent molecular masses of 28, 32, 36, and 42 kDa that bind to HEp-2 cells. A C. jejuni gene encoding a 28 kDa protein, termed PEB1, has been identified and has been proposed to be an adhesin (Pei et al., 1991; Blaser et al., U.S. Pat. No. 5,470,958; Pei and Blaser, 1993). PEB1 shares homology with periplasmic binding proteins involved in nutrient acquisition (Garvis et al., 1996). However, the specific roles of these various proteins in binding and their respective ligands on C. jejuni or C. coli binding to host cells remain unclear.
Many pathogenic microorganisms are capable of binding to components of the extracellular matrix (ECM), such as fibronectin (Fn), laminin, vitronectin, and collagen and may use such interactions during the initial phases of infection. Protozoan parasites such as Leishmania and Trypanosoma cruzi (Wyler, 1987), viral pathogens including hepatitis A and influenza A (Keski-Oja et al., 1987), and bacterial pathogens including Treponema denticola (Dawson and Ellen, 1990; Thomas et al., 1986), Streptococcus pyogenes (Myhre and Kuusela, 1983), Staphlococcus aureus (Kuusela, 1978), Salmonella enteriditis (Baloda et al., 1985), and enterotoxigenic Escherichia coli (Froman et al., 1984) have all been shown to bind to Fn. More recently, C. jejuni has been also reported to bind to Fn and other ECM components (Kuusela et al., 1989; Moser and Schroder, 1995).
There are many possible sources of infection with C. jejuni and C. coli , as they are part of the normal intestinal flora in a wide range of birds and mammals. Large scale outbreaks of human campylobacteriosis have been reported which are usually linked to the consumption of polluted water and raw milk. Pets, especially cats, also can carry these organisms. Sporadic cases of campylobacteriosis are more common and are associated with the consumption of undercooked chicken. As few as 500 Campylobacter organisms are believed to be capable of causing disease. In the United States, case-control studies have attributed 48-70% of the sporadic infections with the consumption of Campylobacter-contaminated chickens. A recent report, using 1,000 fresh chickens bought at grocery stores in 36 cities, revealed that 63% of the chickens tested harbored Campylobacter spp. (Consumer Reports 63:12-18, 1998). This finding is not surprising given the potential for chickens to be heavily cross-contaminated during mechanized processing. Hence, methods for the rapid detection of Campylobacter spp. in foods and for their diagnosis in patients are needed.